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[Title] Selective KIT inhibitor KI-328 and HSP90 inhibitor show different potency against the type of KIT mutations recurrently identified in acute myeloid leukemia.

Activating mutations of KIT play an important role in the pathophysiology of several human malignancies, including acute myeloid leukemia.

Here we examined the potency of a novel KIT inhibitor KI-328 against different types of mutant KIT kinases recurrently identified in AML.

Furthermore, HSP90 inhibitors suppress the growth of D816V-KIT-expressing cells at the concentration at which the growth of other mutant-KIT-expressing cells is not affected.

[MeSH-major] Antineoplastic Agents / pharmacology. Carbamates / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Mutation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Pyrimidines / pharmacology

[MeSH-minor] Cell Line, Tumor. Humans. K562 Cells

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(PMID = 20890793.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbamates; 0 / HSP90 Heat-Shock Proteins; 0 / KI 328; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

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[Title] Myeloid sarcoma of the prostate revealed by urinary retention: a case report.

Myeloid sarcoma (MS) of the prostate is very uncommon with only 17 reported cases in the literature.

Here, a singular case of a MS of the prostate discovered through investigations for urinary retention and revealing an acute leukaemia classified as an acute myeloid leukaemia (AML) with inversion 16 (inv16) according to the World Health Organization (WHO) classification (AML-M4 with inv16 in the French-American-British (FAB) classification) in a 65-year-old man is presented.

None of the previously reported and reviewed cases of prostatic MS were of AML-M4 type.

Such a translocation was recently described in some acute myeloid processes.

Radiation therapy could be beneficial for the localised disease of the prostate.

Allogenic haematopoietic stem cell transplantation is also a promising therapy for MS.

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(PMID = 21686890.001).

[ISSN] 1757-790X

[Journal-full-title] BMJ case reports

[ISO-abbreviation] BMJ Case Rep

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC3029613

   

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[Title] beta-Tryptase up-regulates vascular endothelial growth factor expression via proteinase-activated receptor-2 and mitogen-activated protein kinase pathways in bone marrow stromal cells in acute myeloid leukemia.

Tryptases are predominantly mast cell-specific serine proteases with pleiotropic biological activities.

Recently, significant amounts of tryptases have been shown to be produced by myeloblasts in certain patients with acute myeloid leukemia (AML), but the function of secreted tryptases in pathological circumstances remains unknown.

In this study, we investigated whether beta-tryptase affects the expression of vascular endothelial growth factor (VEGF) in bone marrow stromal cells (BMSCs) in AML.

We detected the expression of proteinase-activated receptor-2 (PAR-2) on AML BMSCs and found that beta-tryptase significantly up-regulated VEGF mRNA and protein expression in a dose-dependent manner by real-time PCR, Western blot, and ELISA.

These results suggest that beta-tryptase up-regulates VEGF production in AML BMSCs via the PAR-2, ERK1/2, and p38MAPK signaling pathways.

[MeSH-major] Bone Marrow Cells / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Promyelocytic, Acute / metabolism. Mitogen-Activated Protein Kinases / metabolism. Receptor, PAR-2 / metabolism. Stromal Cells / metabolism. Tryptases / metabolism. Vascular Endothelial Growth Factor A / metabolism

[MeSH-minor] Blotting, Western. Cell Proliferation. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoenzyme Techniques. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Up-Regulation

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(PMID = 20578818.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptor, PAR-2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.21.59 / Tryptases

   

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[Title] Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.

DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in leukemia pathophysiology.

Its impact in leukemia progression is not fully understood.

We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.

We assessed the methylation status of these genes and of the repetitive element LINE-1 in 30 patients with AML, both at diagnosis and relapse.

Abnormal methylation was found in 23% to 83% of patients at diagnosis and in 47% to 93% at relapse, with CDH13 being the most frequently methylated.

We observed concordance in methylation of several genes, confirming the presence of a hypermethylator pathway in AML.

DNA methylation levels increased at relapse in 25 of 30 (83%) patients with AML.

These changes represent much larger epigenetic dysregulation, since methylation microarray analysis of 9008 autosomal genes in 4 patients showed hypermethylation ranging from 5.9% to 13.6% (median 8.3%) genes at diagnosis and 8.0% to 15.2% (median 10.6%) genes in relapse (P < .001).

Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.

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(PMID = 18523155.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ PMC2515110

   

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[Title] Glutathione S-transferase A1 polymorphisms and acute graft-vs.-host disease in HLA-matched sibling allogeneic hematopoietic stem cell transplantation.

We assessed whether the clinical outcomes, including acute graft-vs.-host disease, of 61 patients with hematological malignancies, following HLA-matched sibling allogeneic stem cell transplantation using busulfan/cyclophosphamide conditioning are altered by glutathione S-transferase A1 genotypes.

Globally, grade II-IV acute graft-vs.-host disease developed in 13 patients (21%).

Grade II-IV acute graft-vs.-host disease developed in 15.2% of 46 patients with GSTA1*A/*A diplotype and in 40.0% of 15 patients with GSTA1*A/*B or GSTA1*B/*B diplotype (p = 0.04).

Moreover, this relationship between GSTA1*A/*A diplotypes and lower incidence of acute graft-vs.-host disease was independent of the age, gender, stem cell source, and disease status.

The incidences of acute skin graft-vs.-host disease were 7% (3/46) in patients with GSTA1*A/*A and 27% (4/15) in patients without GSTA1*A/*A (p = 0.009, univariate; p = 0.01, multivariate).

Acute hepatic graft-vs.-host disease developed in 6 (13%) of 46 patients with the GSTA1*A/*A diplotype and in 4 (27%) of 15 patients without this diplotype (p = 0.09, univariate; p = 0.12, multivariate).

Ten patients (16%) developed hepatic veno-occlusive disease.

No significant difference was found in the incidence of hepatic veno-occlusive disease between patients with and without the GSTA1*A/*A diplotype (19.6% vs. 6.7%; p = 0.24).

We conclude that the GSTA1*A/*A diplotype is an independent protective factor against acute graft-vs.-host disease, especially for skin graft-vs.-host disease, and probably for hepatic graft-vs.-host disease, in patients using busulfan/cyclophosphamide conditioning.

The identification of glutathione S-transferase A1 genotypes prior to allogeneic stem cell transplantation could allow conditioning regimens and graft-vs.-host disease prophylaxis to be modified to improve outcome.

[MeSH-major] Glutathione Transferase / genetics. Graft vs Host Disease / genetics. Hematopoietic Stem Cell Transplantation. Polymorphism, Single Nucleotide

[MeSH-minor] Acute Disease. Adult. Female. Genotype. Hepatic Veno-Occlusive Disease / etiology. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid / surgery. Male. Middle Aged. Siblings. Transplantation Conditioning

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(PMID = 17425746.001).

[ISSN] 0902-0063

[Journal-full-title] Clinical transplantation

[ISO-abbreviation] Clin Transplant

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] EC 2.5.1.18 / GSTA1 protein, human; EC 2.5.1.18 / Glutathione Transferase

   

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[Title] Genetic parameter estimates of meat quality traits in Duroc pigs selected for average daily gain, longissimus muscle area, backfat thickness, and intramuscular fat content.

Using a multitrait animal model BLUP, selection was conducted over seven generations for growth rate (ADG), real-time ultrasound LM area (LMA), backfat thickness (BF), and intramuscular fat content (IMF) to develop a new line of purebred Duroc pigs with enhanced meat production and meat quality.

Genetic correlations of IMF with ADG and BF were low and positive, but low and negative with LMA.

Tenderness was correlated negatively with ADG (-0.44) and BF (-0.59), but positively correlated with LMA (0.32).

The genetic correlation between LMA and DL was positive and high (0.64).

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(PMID = 16100060.001).

[ISSN] 1525-3163

[Journal-full-title] Journal of animal science

[ISO-abbreviation] J. Anim. Sci.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9007-34-5 / Collagen

   

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[Title] Allogeneic stem cell transplantation in children with leukemia using human leukocyte antigen-mismatched unrelated donors.

Allogeneic HSCT is a curative treatment, when chemotherapy fails, for certain malignant diseases.

We present our data of HSCT using HLA partially allele-mismatched (7-8/10) UDs in 24 children with leukemia.

Acute GvHD grade II was diagnosed in 70.8% of the patients and grade III-IV in 12.5%.

It enables stable engraftment, good control of GvHD, full reconstitution of immunity, and is not connected with unacceptable transplant-related mortality.

[MeSH-major] Graft vs Host Disease / prevention & control. Leukemia / surgery. Stem Cell Transplantation

[MeSH-minor] Adolescent. Antilymphocyte Serum / therapeutic use. Bone Marrow Transplantation. Child. Child, Preschool. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Male. Tissue Donors. Transplantation Immunology

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(PMID = 18186885.001).

[ISSN] 1397-3142

[Journal-full-title] Pediatric transplantation

[ISO-abbreviation] Pediatr Transplant

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / Antilymphocyte Serum

   

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[Title] Safe and feasible outpatient treatment following induction and consolidation chemotherapy for patients with acute leukaemia.

Traditionally, patients with acute leukaemia are admitted to hospital during chemotherapy-induced pancytopenia, although a few recent reports have reported the feasibility and safety of outpatient treatment.

We have developed an outpatient treatment programme for patients with acute leukaemia incorporating comprehensive patient education for self-care management at home during pancytopenia and involvement of patients in care of their tunnelled central venous catheter (CVC).

Herein, we report the results of outpatient treatment of 60 patients with acute leukaemia (54 with acute myeloid leukaemia) followed prospectively in the period from March 2004 to 2007.

We conclude that outpatient treatment of patients with acute leukaemia is feasible and safe.

[MeSH-major] Ambulatory Care / methods. Anti-Infective Agents / administration & dosage. Leukemia / drug therapy. Neutropenia / drug therapy. Pancytopenia / drug therapy

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Female. Humans. Male. Middle Aged. Prospective Studies

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(PMID = 20002732.001).

[ISSN] 1600-0609

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Infective Agents

   

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[Title] Molecular and chromosomal alterations: new therapies for relapsed acute myeloid leukemia.

Acute myeloid leukemia (AML) remains the most common form of leukemia and the most common cause of leukemia death.

Although conventional chemotherapy can cure between 25 and 45% of AML patients, the majority of patients die after relapse or of complications associated with treatment.

Thus, more specific and less toxic treatments for AML patients are needed, especially for elderly patients.

An indispensable prerequisite to investigate tailored approaches for AML is the recent progress in the understanding the molecular features that distinguish leukemia progenitors from normal hematopoietic counterparts and the identification of a variety of dysregulated molecular pathways.

In this review, we describe some of the signaling pathways that are aberrantly regulated in AML, with a specific focus on their pathogenetic and therapeutic significance, and we examine some recent therapies directed against these targets, used in clinical trial for relapsed patients or unfit for conventional chemotherapy.

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Signal Transduction / drug effects

[MeSH-minor] Antineoplastic Agents / pharmacology. Drug Design. Genetic Predisposition to Disease / genetics. Humans. Immunologic Factors / pharmacology. Remission Induction. Translocation, Genetic

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(PMID = 18534059.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases

[Number-of-references] 126

   

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BACKGROUND: Patients with neutropenia resulting from chemotherapy for acute myelogenous leukemia or the myelodysplastic syndrome are at high risk for difficult-to-treat and often fatal invasive fungal infections.

CONCLUSIONS: In patients undergoing chemotherapy for acute myelogenous leukemia or the myelodysplastic syndrome, posaconazole prevented invasive fungal infections more effectively than did either fluconazole or itraconazole and improved overall survival.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Female. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality. Male. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / mortality. Single-Blind Method. Treatment Outcome

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[Copyright] Copyright 2007 Massachusetts Medical Society.

[CommentIn] Nat Clin Pract Oncol. 2007 Sep;4(9):512-3 [17646862.001]

[CommentIn] Curr Infect Dis Rep. 2007 Nov;9(6):446-7 [17999879.001]

[CommentIn] N Engl J Med. 2007 May 24;356(21):2215; author reply 2215-8 [17526089.001]

[CommentIn] N Engl J Med. 2007 May 24;356(21):2214-5; author reply 2215-8 [17526090.001]

[CommentIn] N Engl J Med. 2007 May 24;356(21):2214; author reply 2215-8 [17522407.001]

[CommentIn] N Engl J Med. 2007 Jan 25;356(4):409-11 [17251538.001]

(PMID = 17251531.001).

[ISSN] 1533-4406

[Journal-full-title] The New England journal of medicine

[ISO-abbreviation] N. Engl. J. Med.

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00044486

[Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 304NUG5GF4 / Itraconazole; 6TK1G07BHZ / posaconazole; 8VZV102JFY / Fluconazole

   

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[Title] Prognostic significance of FLT3 mutations in pediatric non-promyelocytic acute myeloid leukemia.

This is the first study of FLT3 mutations in pediatric non-promyelocytic AML patients that received the same treatment scheme in single institute.

Patients with FLT3/TKD remain alive after autologous stem cell transplantation.

The disease-free survival (DFS) of patients with FLT3/ITD (0%) was significantly lower than that of the others (52%).

New therapeutic scheme such as stem cell transplantation with more intensive conditioning just after complete remission could be applied in pediatric non-promyelocytic AML patients with the FLT3/ITD mutation.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics

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(PMID = 15863200.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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[Title] Feverfew: weeding out the root of leukaemia.

Malignant stem cells are central to the pathogenesis and perpetuation of acute myelogenous leukaemia (AML).

Despite their crucial role, standard chemotherapy often does not target these critical cells and, thus, the 'root' of leukaemic disease is not eradicated.

To derive better therapies, unique molecular features of malignant stem cells have been characterised for AML and evaluated with regard to ablation of disease.

In the course of such studies, the compound parthenolide, which is derived from the medicinal plant feverfew, has recently been shown to preferentially induce AML stem cells to undergo apoptosis.

Thus, this naturally occurring agent may provide new avenues of investigation for the treatment of leukaemia.

[MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Neoplastic Stem Cells / drug effects. Sesquiterpenes / pharmacology. Tanacetum parthenium / chemistry

[MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Humans. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Plants, Medicinal / chemistry. Xenograft Model Antitumor Assays

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(PMID = 16120045.001).

[ISSN] 1744-7682

[Journal-full-title] Expert opinion on biological therapy

[ISO-abbreviation] Expert Opin Biol Ther

[Language] eng

[Publication-type] Editorial

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide

   

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[Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.

Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).

So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.

In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).

Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.

[MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics

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(PMID = 19357396.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human

   

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[Title] JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.

The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).

JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic myelogenous leukemia (CML), 2 (18%) of 11 patients with megakaryocytic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with myelodysplastic syndromes.

No mutation was found in Ph(+)CML (99 patients), AML M0-M6 (28 patients), or acute lymphoblastic leukemia (20 patients).

We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but not critical for transformation to the acute phase of these diseases and that it is generally rare in aggressive leukemias.

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[Cites] Anal Biochem. 2000 Apr 10;280(1):103-10 [10805527.001]

[Cites] Blood. 2005 Sep 15;106(6):2162-8 [15920007.001]

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(PMID = 16037387.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50CA100632

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2

[Other-IDs] NLM/ PMC1895065

   

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[Title] Optimizing the classification of acute lymphoblastic leukemia and acute myeloid leukemia samples using artificial neural networks.

Accurate classification of human blood cells plays a decisive role in the diagnosis and treatment of diseases.

Artificial Neural Networks (ANN) have been consistently used as a trusted classification tool for this type of analysis.

In this study, a new Artificial Neural Network approach is proposed for the multidimensional classification of two of the most common forms of leukemia: Acute Lymphoblastic Leukemia (ALL) and Acute Myeloid Leukemia (AML), also sometimes called Acute Myelogenous Leukemia.

The goal was to establish a programming tool, supported through this new ANN development, for the identification of normal and abnormal blood samples and provide information to medical doctors in the form of diagnostic references for the specific disease state that is considered for this study.

The application of the ANN algorithm produced remarkable classification accuracy results that show a 95% classification accuracy for the normal blood samples and 90% classification accuracy for the abnormal samples even under the ubiquitous problem of overlap.

[MeSH-major] Blood Cell Count / methods. Diagnosis, Computer-Assisted / methods. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Neural Networks (Computer). Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Blood Cells / classification. Cluster Analysis. Humans. Pattern Recognition, Automated / methods. Quality Control. Reproducibility of Results. Sensitivity and Specificity

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(PMID = 16817618.001).

[ISSN] 0067-8856

[Journal-full-title] Biomedical sciences instrumentation

[ISO-abbreviation] Biomed Sci Instrum

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

   

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[Title] Is age an independent risk factor for chemically induced acute myelogenous leukemia in children?

Secondary or therapy-related acute myelogenous leukemia (t-AML) is a rare but unfortunate consequence of treatment with certain classes of cytotoxic chemotherapeutic agents or chronic exposure to high concentrations of benzene.

Drugs known to produce AML following chemotherapy of primary malignancy are usually alkylating agents or topoisomerase II inhibitors.

Both children and adults develop AML following treatment with these classes of antineoplastic drugs.

In this review, the effect of age at treatment on a child's susceptibility to developing therapy related AML was investigated.

As demonstrated in the published literature, the risk of developing AML following chemotherapy is not reliably correlated with the age of the pediatric patient.

For example, secondary solid tumors such as breast, central nervous system (CNS), bone, and thyroid cancer are highly dependent on the age of the patient at time of diagnosis and treatment; in contrast, an age dependency for t-AML risk was not observed in these same patient populations.

Predictably, the induction of t-AML in children follows a rational dose-response relationship, with increasing doses of chemotherapy resulting in greater risk. Recent U.S.

Available scientific and medical literature does not support the hypothesis that children necessarily possess an increased risk of developing AML following leukemogenic chemical exposure.

[MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Neoplasms, Second Primary / epidemiology

[MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Disease Susceptibility. Humans. Risk Factors. Topoisomerase II Inhibitors

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(PMID = 17687725.001).

[ISSN] 1521-6950

[Journal-full-title] Journal of toxicology and environmental health. Part B, Critical reviews

[ISO-abbreviation] J Toxicol Environ Health B Crit Rev

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors

[Number-of-references] 92

   

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[Title] Acute myeloid leukaemia diagnosed by intra-oral myeloid sarcoma. A case report.

Myeloid sarcoma (MS) is a rare extramedullary malignant tumor composed of immature myeloid cells.

It is strongly associated with a well known or covert acute myeloid leukaemia, chronic myeloproliferative diseases or myelodysplastic syndromes.

An unusual case of acute myeloid leukaemia, which was diagnosed by mandibular MS that was developed in the alveolar socket after a dental extraction, is reported.

The histological examination (including immunohistochemical analysis) of a subsequent biopsy showed infiltration of the oral mucosa by neoplastic cells.

This lesion was therefore classified as acute myeloid leukaemia.

The patient was referred to oncologists that confirmed the initial diagnosis.

Forty days later, a relapse of the disease, which appeared as a great-ulcerated lesion, was developed in the hard palate.

Review of the literature shows no report of intraoral relapse and particularly multiple relapse of a MS that involves the oral cavity.

Even though MS is encountered infrequently in the oral cavity, it should be considered in the differential diagnosis of conditions (especially tumors) with a similar clinical appearance.

[MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis. Sarcoma, Myeloid / diagnosis

[MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy. Diagnosis, Differential. Etoposide / therapeutic use. Fatal Outcome. Female. Humans. Mouth Mucosa / pathology. Mouth Neoplasms

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[Cites] J Oral Maxillofac Surg. 1990 Jul;48(7):748-52 [2193130.001]

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(PMID = 20512638.001).

[ISSN] 1936-0568

[Journal-full-title] Head and neck pathology

[ISO-abbreviation] Head Neck Pathol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 6PLQ3CP4P3 / Etoposide

[Other-IDs] NLM/ PMC2878628

   

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[Title] Wilms tumor 1 gene mutations are associated with a higher risk of recurrence in young adults with acute myeloid leukemia: a study from the Acute Leukemia French Association.

BACKGROUND: Wilms tumor 1 (WT1) is a transcription factor that is overexpressed in most acute myeloid leukemias (AMLs).

Recently, 2 groups reported that WT1 mutations occur in approximately 10% of normal karyotype AMLs and are an independent predictor of poor outcome in this subgroup of patients with AML.

METHODS: The authors studied a cohort of 268 young adults (ages 15-50 years) with AML who were treated on the Acute Leukemia French Association 9802 trial.

Within the subgroup of patients who had normal karyotype AML (n = 106), WT1 mutation was identified as an independent adverse prognostic factor for the risk of recurrence.

CONCLUSIONS: The current results indicted that WT1 mutations represent an adverse prognostic factor in young adults with AML.

Prospective trials should confirm the clinical relevance of WT1 mutations in relation to other prognostic factors in patients with AML.

[MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics

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(PMID = 19536888.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

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[Title] Overexpression of CDX2 perturbs HOX gene expression in murine progenitors depending on its N-terminal domain and is closely correlated with deregulated HOX gene expression in human acute myeloid leukemia.

The mechanisms underlying deregulation of HOX gene expression in AML are poorly understood.

Deletion of the N-terminal domain of Cdx2 abrogated its ability to perturb Hox gene expression and to cause acute myeloid leukemia (AML) in mice.

In contrast inactivation of the putative Pbx interacting site of Cdx2 did not change the leukemogenic potential of the gene.

In an analysis of 115 patients with AML, expression levels of CDX2 were closely correlated with deregulated HOX gene expression.

All patients with AML with normal karyotype tested were negative for CDX1 and CDX4 expression.

They furthermore correlate the level of CDX2 expression with HOX gene expression in human AML and support a potential role of CDX2 in the development of human AML with aberrant Hox gene expression.

[MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Transcription Factors / genetics

[MeSH-minor] Adult. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / physiology. Bone Marrow Transplantation. Cell Line, Tumor. Gene Expression Profiling. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Humans. Karyotyping. Mice. Mutagenesis. NIH 3T3 Cells. Protein Structure, Tertiary. Translocation, Genetic. Up-Regulation / physiology

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(PMID = 17855634.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors

   

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[Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].

OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.

METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.

RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.

The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.

21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.

21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.

17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.

CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.

21) (q22; q22)/AML-ETO fusion gene and t (15;.

[MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics

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(PMID = 16321221.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1

   

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Most of these patients are ventilated through endotracheal tubes (ETTs), others through laryngeal mask airways (LMAs).

The cuffs of both ETTs and LMAs inflate with increases in altitude as barometric pressure decreases (30 mbar/1000 feet).

METHODS: The change in dimensions of the inflated cuffs of a size 8 ETT and a size 5 LMA were measured with digital callipers at 1000 feet intervals in the unpressurised cabin of an Agusta 109 helicopter used by the Warwickshire and Northamptonshire Air Ambulance.

RESULTS: A linear expansion in cuff dimensions as a function of altitude increase was identified.

CONCLUSION: The data for LMA cuff expansion failed to show significant correlation with altitude change.

Further work is required to determine a similar rule of thumb for LMA cuff deflation.

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[Cites] Anaesthesia. 2000 Dec;55(12):1179-84 [11121927.001]

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(PMID = 17351218.001).

[ISSN] 1472-0213

[Journal-full-title] Emergency medicine journal : EMJ

[ISO-abbreviation] Emerg Med J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2660019

   

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[Title] Spinal osteomyelitis due to Aspergillus flavus in a child: a rare complication after haematopoietic stem cell transplantation.

We report the case of a child affected by acute myeloid leukaemia who was treated with allogeneic haematopoietic stem cell transplantation and developed cervicothoracic spinal osteomyelitis due to Aspergillus flavus.

The diagnosis was difficult on a clinical basis, but made possible by conventional radiography and MRI.

[MeSH-major] Aspergillosis / complications. Hematopoietic Stem Cell Transplantation / adverse effects. Osteomyelitis / microbiology. Spinal Diseases / microbiology

[MeSH-minor] Aspergillus flavus / isolation & purification. Bronchoalveolar Lavage. Diagnosis, Differential. Fatal Outcome. Fever / etiology. Humans. Hydrocephalus / etiology. Infant. Leukemia, Myeloid, Acute / surgery. Magnetic Resonance Imaging. Male. Radiography. Rare Diseases. Recurrence. Spine / diagnostic imaging. Spine / pathology

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[Cites] Pediatr Radiol. 2003 Jul;33(7):453-60 [12739082.001]

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(PMID = 18392819.001).

[ISSN] 0301-0449

[Journal-full-title] Pediatric radiology

[ISO-abbreviation] Pediatr Radiol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

   

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[Title] Drug delivery in acute myeloid leukemia.

BACKGROUND: Acute myeloid leukemia was among the first malignancies to be cured by drug therapy alone, but overall survival rates remain unsatisfactory and have changed little over the past 20 years.

OBJECTIVE: We have chosen acute myeloid leukemia as a disease prototype to review established and novel targeted approaches in leukemia treatment.

CONCLUSION: While the toxicity profile of chemotherapeutics has been improved by liposomal formulations and antibody conjugation for leukemia-directed uptake, their efficacy has probably not changed significantly.

Further improvements may result from the characterization of novel acute myeloid leukemia (AML) cell surface receptors and of leukemic stem cells, as well as from the design of leukemia-targeted gene therapy vectors.

[MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Drug Delivery Systems. Genetic Therapy. Humans. Integrin alpha4beta1 / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Liposomes. Neoplastic Stem Cells / drug effects. Sialic Acid Binding Ig-like Lectin 3

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(PMID = 18532921.001).

[ISSN] 1742-5247

[Journal-full-title] Expert opinion on drug delivery

[ISO-abbreviation] Expert Opin Drug Deliv

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Integrin alpha4beta1; 0 / Liposomes; 0 / Sialic Acid Binding Ig-like Lectin 3

[Number-of-references] 114

   

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[Title] Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.

EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of acute myeloid leukemia (AML) patients.

RESULTS: The antibody did not impair the growth of MOLT-4 and U-937 cells in culture.

Its conjugate with curcumin, however, was lethal to both cell lines.

The immunoconjugate killed tumor cells bearing the CD33 marker of an AML patient expressing hCGbeta but did not have a similar action on cells of another AML patient with the CD13 marker but who was negative for hCGbeta.

[MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism. Leukemia / drug therapy. Lymphoma / drug therapy

[MeSH-minor] Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Cell Separation. Drug Design. Female. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells

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(PMID = 19127081.001).

[ISSN] 1423-0232

[Journal-full-title] Oncology

[ISO-abbreviation] Oncology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin

   

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[Title] Achyrocline satureioides (LAM.) DC (Marcela): antimicrobial activity on Staphylococcus spp. and immunomodulating effects on human lymphocytes.

Achyrocline satureioides (LAM.

They were isolated from 18 patients with acne lesions and from 7 patients infected with Staphylococcus spp. (5 strains were taken from catheters and 2 from wounds).

On the other hand, cultures of lymphocytes were made from those patients who displayed infections caused by Staphylococcus spp. and from 12 control non-infected individuals.

The A. satureiodes decoction inhibited 95% of the isolated Staphylococcus spp. strains and stimulated the lymphocyte expansion, of which 40% were CD8+ T cells.

[MeSH-minor] Acne Vulgaris / microbiology. Adolescent. Adult. Bacteremia / microbiology. Catheterization. Cells, Cultured / drug effects. Drug Evaluation, Preclinical. Humans. Lymphocyte Activation / drug effects. Phytohemagglutinins / pharmacology. Plant Leaves / chemistry. Staphylococcal Infections / microbiology. Staphylococcal Skin Infections / microbiology. Wound Infection / microbiology

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(PMID = 18293658.001).

[ISSN] 0187-4640

[Journal-full-title] Revista latinoamericana de microbiología

[ISO-abbreviation] Rev. Latinoam. Microbiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Mexico

[Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Anti-Bacterial Agents; 0 / Phytohemagglutinins; 0 / Plant Extracts

   

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[Title] Volatile components of Centaurea eryngiodes Lam. and Centaurea iberica Trev.var. hermonis Bois. Lam.,two Asteraceae growing wild in Lebanon.

The volatile components of the flowerheads of Centaurea eryngioides Lam. and Centaurea iberica Trev. var. hermonis Boiss. Lam. were obtained by hydrodistillation and identified by GC and GC-MS.

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(PMID = 16317829.001).

[ISSN] 1478-6419

[Journal-full-title] Natural product research

[ISO-abbreviation] Nat. Prod. Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Oils, Volatile; 0 / Plant Oils

   

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[Title] Detailed analysis of FLT3 expression levels in acute myeloid leukemia.

BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of acute myeloid leukemia (AML).

DESIGN AND METHODS: To further evaluate the role of FLT3 in AML we investigated FLT3 expression levels in 207 adult AML patients and 8 healthy donors by real-time polymerase chain reaction (PCR).

RESULTS: FLT3 expression levels were different in certain FAB types with increasing levels in the following order: M3<M3v<M6<M2<M4eo<M4<M0<M1<M5a<M5b.

Independent analysis of FLT3 expression in cytogenetic AML subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive AML.

On the molecular level, no differences in FLT3 expression levels were detected between AML with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).

In patients with normal cytogenetics no impact or overall survival or event-free survival could be detected (p=0.128 and p=0.305, respectively) regardless of FLT3 muatation status, whereas investigating the group of patients with normal cytogenetics and wild-type FLT3, a clear tendency for a worse overall (p=0.059) and event free (p=0.087) survival was found.

[MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Disease-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences

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[CommentIn] Haematologica. 2005 Dec;90(12):1586 [16330422.001]

(PMID = 16330434.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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[Title] Peripheral blasts on day 21 of induction chemotherapy in a patient with core binding factor acute myeloid leukemia: more than meets the eye.

The combination of fludarabine, high-dose cytarabine, gemtuzumab ozogamicin, and granulocyte colony-stimulating factor (G-CSF), the FLAG-GO protocol, has resulted in excellent response rates and superior relapse-free survival as first-line therapy for patients with core binding factor acute myeloid leukemia (AML).

A side effect of administration of G-CSF is an increase in peripheral white blood cell count and blast cell percentage during the recovery phase of the bone marrow after induction chemotherapy.

A 60-year-old man with inversion 16 AML was admitted for induction chemotherapy with the FLAG-GO protocol at our institution.

Our case report underscores the importance of recognizing this phenomenon associated with the administration of G-CSF, and waiting for 5-7 days before administering re-induction therapy or classifying the disease as primary refractory AML.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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(PMID = 20709669.001).

[ISSN] 2152-2669

[Journal-full-title] Clinical lymphoma, myeloma & leukemia

[ISO-abbreviation] Clin Lymphoma Myeloma Leuk

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FLAG protocol

   

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With regard to hematological malignancies a stimulating effect of VEGF for proliferation, survival and migration of leukemia cells could be demonstrated.

Bone marrow of leukemia patients shows an increased microvessel density as well as VEGF expression.

Complete remissions in acute myeloid leukemia (AML) have been reported by targeting the receptor tyrosine kinase system of VEGF.

While the pathophysiology behind the contribution of VEGF to leukemia progression is not yet completely understood, VEGF and its receptors may provide promising targets not only in solid tumors but also hematological malignancies such as AML.

[MeSH-minor] Cell Proliferation. Cell Survival. Disease Progression. Humans

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(PMID = 17305503.001).

[ISSN] 1873-5592

[Journal-full-title] Current drug targets

[ISO-abbreviation] Curr Drug Targets

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor

[Number-of-references] 226

   

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[Title] Successful treatment of disseminated mucormycosis with a combination of liposomal amphotericin B and posaconazole in a patient with acute myeloid leukaemia.

[MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Leukemia, Myeloid, Acute / complications. Liposomes / therapeutic use. Mucormycosis / drug therapy. Rhizomucor / isolation & purification. Triazoles / therapeutic use

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(PMID = 16961579.001).

[ISSN] 0933-7407

[Journal-full-title] Mycoses

[ISO-abbreviation] Mycoses

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Liposomes; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B

   

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Their response to "missing self" signals was described 3 decades ago, but the recent discovery of a panoply of activating receptors has made it clear that NK cell reactivity arises from a combination of inhibitory and activating signals.

Successful clinical exploitation of NK cell reactivity was demonstrated in allogeneic transplantation for acute myelogenous leukemia from HLA-haploidentical donors when matched donors were not available.

This review summarizes the heterogeneous clinical results and explains them based on a succinct description of NK cell biology.

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(PMID = 19539207.001).

[ISSN] 1523-6536

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA18029; United States / NIAID NIH HHS / AI / T32 AI007290; United States / NCI NIH HHS / CA / R01 CA125276-02; United States / NCI NIH HHS / CA / CA125276-02; United States / NCI NIH HHS / CA / R01 CA125276

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] United States

[Number-of-references] 139

[Other-IDs] NLM/ NIHMS205040; NLM/ PMC2884143

   

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[Title] RUNX1 DNA-binding mutants, associated with minimally differentiated acute myelogenous leukemia, disrupt myeloid differentiation.

Mutations in the RUNX1 gene are found at high frequencies in minimally differentiated acute myelogenous leukemia.

Significantly, the RDB mutants did not act in a transdominant fashion in vivo to disrupt Runx1 activity in either T-cell or platelet development, which are highly sensitive to Runx1 dosage.

Disruption of the interface that binds CBFbeta, an important cofactor of Runx1, did not impair RDB mutant replating activity, arguing against inactivation of Runx1 function by CBFbeta sequestration.

[MeSH-major] Cell Differentiation / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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(PMID = 17234761.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / RUNX1 protein, human

   

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[Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].

OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.

METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.

The cell cycle was examined by flow cytometric analysis.

(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).

CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.

Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.

[MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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(PMID = 16029562.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger

   

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[Title] I kappa B-mediated apoptotic gene therapy against acute myelogenous leukemia using replication-defective HSV-1 vector expressing TK and mutant I kappa B alpha.

Overexpression of NF-kappa B reportedly plays anti-apoptotic roles in the growth of AML cells.

Control of AML cell growth was attempted using a replication-defective herpes simplex virus-1 vector, T0I kappa B alpha, overexpressing mutant I kappa B alpha to inhibit NF-kappa B in vitro.

Infection of T0I kappa B alpha at 15 multiplicity of infection (MOI) with cells of AML lines, HL60, K562, and NB4 displaying >90% infection efficiency and tumor killing in vitro.

Fresh AML cells from 8 patients were infected with T0I kappa B alpha at 3 MOI, with or without GCV or 10 microM of Ara-C in vitro.

Our results suggest that T0I kappa B alpha-mediated gene therapy induces apoptosis of AML cells in vitro.

[MeSH-major] Apoptosis. Genetic Therapy. Herpesvirus 1, Human / genetics. I-kappa B Kinase / metabolism. I-kappa B Proteins / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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(PMID = 16171566.001).

[ISSN] 1165-158X

[Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)

[ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] France

[Chemical-registry-number] 0 / I-kappa B Proteins; EC 2.7.1.21 / Thymidine Kinase; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspase 3; P9G3CKZ4P5 / Ganciclovir

   

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[Title] Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia.

To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML).

AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites.

The adoptive transfer of in vitro-generated, potently lytic anti-AML-reactive CTLs failed to reduce disease burden or extend survival.

Compared with non-AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases.

Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival.

In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response.

These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.

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(PMID = 19724059.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA120409-03; United States / NCI NIH HHS / CA / CA120409-03; United States / NCI NIH HHS / CA / R01 CA120409; United States / NCI NIH HHS / CA / R01 CA72669; United States / NHLBI NIH HHS / HL / R01 HL056067; United States / NCI NIH HHS / CA / R01 CA072669

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / interleukin 2-diphtheria toxin

[Other-IDs] NLM/ PMC2773484

   

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[Title] [The diagnosis of acute myeloid leukaemia enhanced by using DNA microarrays].

[Transliterated title] Diagnostiek van acute myeloïde leukemie in een stroomversnelling door toepassing van DNA-microarrays.

Recently, two studies have shown that the use ofgene-expression profiling using DNA microarrays or DNA chips may improve the classification of acute myeloid leukaemia (AML).

In both studies, cluster analyses based on the molecular signatures defined known subgroups as well as novel subgroups of AML.

Chromosomal lesions, mutations, and abnormal gene expression with prognostic value determined the clustering.

In fact, gene-expression profiling recognized leukaemias with certain chromosomal aberrations that had been missed by routine cytogenetics.

Thus, gene-expression profiling allows a comprehensive classification of AML that includes previously-identified genetically-defined as well as novel prognostically-relevant subgroups.

[MeSH-major] Chromosome Aberrations. Gene Expression Profiling / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Oligonucleotide Array Sequence Analysis

[MeSH-minor] Acute Disease. Cluster Analysis. Cytogenetic Analysis. Humans

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[CommentIn] Ned Tijdschr Geneeskd. 2005 Mar 19;149(12):618-22 [15813427.001]

(PMID = 15813428.001).

[ISSN] 0028-2162

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

[Publication-type] English Abstract; Journal Article

[Publication-country] Netherlands

   

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The International Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002).

The time until 25% developed acute myeloid leukemia (AML) was longer in the good and intermediate predictive groups for erythroid response compared with the poor predictive group (52 versus 13 months, P = .008).

Only 1 of 20 long-term responders developed AML.

There was no difference in survival (odds ratio [OR], 0.9; 95% confidence interval [CI], 0.7-1.2; P = .55) or risk of AML evolution (OR, 1.3; 95% CI, 0.7-2.2; P = .40) between treated and untreated patients.

Patients with high/intermediate probability of response and with IPSS Low/Int-1 show frequent and durable responses without adverse effects on outcome, while other patients should not be considered candidates for this treatment.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Analysis of Variance. Cell Transformation, Neoplastic. Female. Humans. Leukemia, Myeloid / etiology. Male. Middle Aged. Predictive Value of Tests. Prognosis. Survival Analysis. Treatment Outcome

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(PMID = 15840690.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor

   

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[Title] The FcgammaRIIa-polymorphic site as a potential target for acute graft-versus-host disease in allogeneic stem cell transplantation.

Graft-versus-host disease (GVHD) is a serious complication of allogeneic stem cell transplantation for hematologic diseases.

Polymorphisms are known for FcgammaRIIa, and this molecule is present on endothelial, dendritic, and Langerhans cells.

Donor cells reacting against the patient as GVHD can also react against the malignancy of the patient, and this is known as the graft-versus-leukemia (GVL) effect.

Because the FcgammaRIIa molecule is also present on acute myeloid leukemia (AML) cells, an FcgammaRIIa mismatch could be a target for both GVHD and GVL.

We retrospectively studied 73 AML patients and analyzed the differences in GVHD and relapse incidence between patients with and without a pro-GVHD/GVL FcgammaRIIa allotype mismatch.

Univariate and multivariate analyses demonstrated the pro-GVHD mismatch to be a significant risk factor for the development of acute GVHD.

The relapse incidence was not significantly different for patients with or without the pro-GVL mismatch, although there was a trend for fewer relapses in standard-risk AML patients with the pro-GVL mismatch.

We conclude that the polymorphism of the FcgammaRIIa receptor may be a candidate target for acute GVHD.

[MeSH-major] Antigens, CD / genetics. Graft vs Host Disease / genetics. Hematopoietic Stem Cell Transplantation / adverse effects. Polymorphism, Genetic. Receptors, IgG / genetics

[MeSH-minor] Acute Disease. Adult. Aged. Analysis of Variance. Cohort Studies. Female. Graft vs Leukemia Effect / genetics. Graft vs Leukemia Effect / immunology. Humans. Incidence. Leukemia, Myeloid / complications. Leukemia, Myeloid / therapy. Male. Middle Aged. Recurrence. Retrospective Studies. Transplantation Immunology. Transplantation, Homologous

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(PMID = 15744239.001).

[ISSN] 1083-8791

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Fc gamma receptor IIA; 0 / Receptors, IgG

   

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[Title] Clinical utility of a commercial LAM-ELISA assay for TB diagnosis in HIV-infected patients using urine and sputum samples.

BACKGROUND: The accurate diagnosis of TB in HIV-infected patients, particularly with advanced immunosuppression, is difficult.

Recent studies indicate that a lipoarabinomannan (LAM) assay (Clearview-TB(R)-ELISA) may have some utility for the diagnosis of TB in HIV-infected patients; however, the precise subgroup that may benefit from this technology requires clarification.

The utility of LAM in sputum samples has, hitherto, not been evaluated.

METHODS: LAM was measured in sputum and urine samples obtained from 500 consecutively recruited ambulant patients, with suspected TB, from 2 primary care clinics in South Africa.

Culture positivity for M. tuberculosis was used as the reference standard for TB diagnosis.

Urine-LAM positivity was associated with HIV positivity (p = 0.007) and test sensitivity, although low, was significantly higher in HIV-infected compared to uninfected patients (21% versus 6%; p<0.001), and also in HIV-infected participants with a CD4 <200 versus >200 cells/mm(3) (37% versus 0%; p = 0.003).

Urine-LAM remained highly specific in all 3 subgroups (95%-100%).

25% of smear-negative but culture-positive HIV-infected patients with a CD4 <200 cells/mm(3) were positive for urine-LAM.

Sputum-LAM had good sensitivity (86%) but poor specificity (15%) likely due to test cross-reactivity with several mouth-residing organisms including actinomycetes and nocardia species.

CONCLUSIONS: These preliminary data indicate that in a high burden primary care setting the diagnostic usefulness of urine-LAM is limited, as a rule-in test, to a specific patient subgroup i.e. smear-negative HIV-infected TB patients with a CD4 count <200 cells/mm(3), who would otherwise have required further investigation.

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(PMID = 20352098.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] ENG

[Grant] None / None / / 89918; Canada / Canadian Institutes of Health Research / / 89918; Canada / Canadian Institutes of Health Research / / MOP-89918; United Kingdom / Medical Research Council / /

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ PMC2844421

   

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[Title] Core binding factor acute myeloid leukemia.

Core binding factor (CBF) acute myeloid leukemia (AML) is cytogenetically defined by the presence of t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), which are found in approximately 15% of all adult de novo AML cases.

Despite this molecular commonality, recent studies have demonstrated differences in genetic, clinical, and prognostic features between t(8;21) and inv(16)/t(16;16) AML, thereby supporting the notion that they represent two distinct biologic and clinical entities.

Furthermore, despite being considered as a more favorable AML risk group, only approximately half of the CBF AML patients are cured with current therapy, indicating the need for improved therapeutic approaches.

This review summarizes the most recent laboratory and clinical discoveries relevant to this subset of AML and how they are being applied for in an effort to improve the cure rate in patients with the disease.

[MeSH-major] Chromosome Inversion. Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Translocation, Genetic

[MeSH-minor] Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Neoplasm, Residual / diagnosis. Prognosis

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(PMID = 18692691.001).

[ISSN] 0093-7754

[Journal-full-title] Seminars in oncology

[ISO-abbreviation] Semin. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors

[Number-of-references] 76

   

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[Title] Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.

BACKGROUND: Therapy-related myeloid neoplasm (t-MN) is a distinct class of acute myeloid leukemia (AML) in the World Health Organization (WHO) classification.

Both AML and acute lymphoblastic leukemia (ALL) may develop after treatment for primary cancer.

Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related acute leukemias (t-AL).

METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed acute leukemia.

Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related AML (t-AML) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).

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[Cites] J Clin Oncol. 2003 Apr 1;21(7):1195-204 [12663705.001]

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(PMID = 21120206.001).

[ISSN] 2092-9129

[Journal-full-title] The Korean journal of hematology

[ISO-abbreviation] Korean J Hematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2983048

[Keywords] NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors

   

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Body weight, 10th rib backfat (BF10), last rib backfat (LRF), and loin muscle area (LMA) were serially measured at 10, 13, 16, 19, 22, 24, and 26 wk of age.

At 26 wk of age, Duroc-sired progeny were heavier (143.4 vs. 132.7 kg, P < 0.001), had more BF10 (27.1 vs. 23.7 mm, P < 0.001) and LRF (21.2 vs. 19.2 mm, P < 0.001), but had similar LMA (46.4 vs. 47.1 cm2) compared with Pietrain-sired progeny.

Mean feed efficiency did not differ between breed of sire in any period of the study.

Random regression animal models with polynomial regression on week on-test were fitted to BW, BF10, LRF, LMA, FFTOLN, TOFAT, EBPRO, and EBLIPID from 10 to 26 wk of age.

Serial heritability estimates generally increased from 10 to 26 wk of age with ranges as follows: BW (0.05 to 0.39), BF10 (0.13 to 0.76), LRF (0.11 to 0.79), LMA (0.05 to 0.73), FFTOLN (0.07 to 0.16), TOFAT (0.19 to 0.45), EBPRO (0.02 to 0.55), and EBLIPID (0.12 to 0.60).

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(PMID = 16424252.001).

[ISSN] 1525-3163

[Journal-full-title] Journal of animal science

[ISO-abbreviation] J. Anim. Sci.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

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[Title] Mucormycosis resulting in gastric perforation in a patient with acute myelogenous leukemia: report of a case.

Mucormycosis is an uncommon opportunistic fungal infection that may develop in immunocompromised patients with conditions such as diabetes mellitus, leukemia, lymphoma, or human immunodeficiency virus (HIV), or after transplantation with immunosupperessive therapy.

We report a case of gastric perforation caused by a mucormycosis infection in a patient with acute myelogenous leukemia (AML).

[MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Gastrectomy. Intestinal Perforation / etiology. Leukemia, Myeloid, Acute / drug therapy. Mucormycosis / complications. Stomach / injuries. Treatment Outcome

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(PMID = 16937290.001).

[ISSN] 0941-1291

[Journal-full-title] Surgery today

[ISO-abbreviation] Surg. Today

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B

   

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Intracellular NAD is essential for cell survival, and NAD depletion resulting from APO866 treatment elicits tumor cell death.

Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel of cell lines (n = 45) and primary cells (n = 32).

Most cancer cells (acute myeloid leukemia [AML], acute lymphoblastic leukemia [ALL], mantle cell lymphoma [MCL], chronic lymphocytic leukemia [CLL], and T-cell lymphoma), but not normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.

The NAD depletion led to cell death.

At 96 hours, APO866-mediated cell death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.

Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human AML, lymphoblastic lymphoma, and leukemia without significant toxicity to the animals.

[MeSH-minor] Animals. Cell Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays

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[CommentIn] Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8 [19498032.001]

(PMID = 19196867.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human

   

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[Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.

Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.

Rearrangements of the MLL gene are found in most cases of infant AML and regardless of age confer an intermediate risk.

The treatment of MLL-rearranged ALL in children involves increased intensification of chemotherapy, and infants with ALL are treated with an intensive regimen of ALL- and AML-like chemotherapy, with the proportion of MLL-rearranged cases being responsible for the poor outcome in this age group.

The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.

It may also prove to have a useful role in both diagnosis and prognosis.

[MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 17905612.001).

[ISSN] 1079-9796

[Journal-full-title] Blood cells, molecules & diseases

[ISO-abbreviation] Blood Cells Mol. Dis.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

[Number-of-references] 82

   

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[Title] Perspectives of proteomics in acute myeloid leukemia.

Acute myeloid leukemia (AML) is a frequent hematological malignancy.

Despite enormous therapeutic efforts that range from various cytotoxic agents to allogeneic stem cell transplantation, overall survival of patients with AML remains unsatisfying.

There is hope that elucidation of the AML-specific proteome will prompt the discovery of novel therapeutic targets and biomarkers in AML.

Modern mass-spectrometry instrumentation has achieved excellent performance in terms of sensitivity, resolution and mass accuracy; however, so far, the contribution of proteomics to the care of patients with AML is virtually zero.

Since mass-spectrometry instruments are very intricate devices, their successful operation will hinge on the willingness and ability of mass-spectrometry experts and clinical researchers to adopt new views, learn from each other and cooperate in order to ultimately benefit the patient suffering from AML.

This review highlights some clinical problems circumventing the treatment of patients with AML.

Furthermore, it provides a brief overview of the technical background of standard proteomics approaches and describes opportunities, challenges and pitfalls of proteomic studies with regards to AML.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Proteomics

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(PMID = 17134369.001).

[ISSN] 1744-8328

[Journal-full-title] Expert review of anticancer therapy

[ISO-abbreviation] Expert Rev Anticancer Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins

[Number-of-references] 99

   

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[Title] Gene mutations and response to treatment with all-trans retinoic acid in elderly patients with acute myeloid leukemia. Results from the AMLSG Trial AML HD98B.

BACKGROUND: In a previous randomized trial, AML HD98B, we showed that administration of all-trans retinoic acid in addition to intensive chemotherapy improved the outcome of older patients with acute myeloid leukemia.

DESIGN AND METHODS: Data from mutation analyses of the NPM1, CEBPA, FLT3, and MLL genes were correlated with outcome in patients 61 years and older treated within the AML HD98B trial.

The genotype mutant NPM1 was positively and adverse cytogenetics as well as higher white blood cell count negatively correlated with achievement of complete remission.

Other significant factors for survival were age, adverse cytogenetics, and logarithm of white cell count.

CONCLUSIONS: In elderly patients with acute myeloid leukemia, NPM1 mutations are associated with achievement of complete remission, and the genotype 'mutant NPM1 without FLT3-ITD' appears to be a predictive marker for response to all-trans retinoic acid given as an adjunct to intensive chemotherapy (ClinicalTrials.gov Identifier: NCT00151242).

[MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Tretinoin / therapeutic use

[MeSH-minor] Aged. Aged, 80 and over. Biomarkers / metabolism. Disease-Free Survival. Female. Humans. Male. Middle Aged. Pilot Projects. Survival Rate. Treatment Outcome

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[CommentIn] Haematologica. 2009 Jan;94(1):10-6 [19118375.001]

(PMID = 19059939.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00151242

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / Biomarkers; 5688UTC01R / Tretinoin

[Other-IDs] NLM/ PMC2625424

[Investigator] Glasmacher A; Mergenthaler HG; Nerl C; Pralle H; Hensel M; Preiss J; Salwender H; Biedermann HG; Kremers S; Griesinger F